Cited by 149Histone Deacetylase Inhibitors ResearchAcute Lymphoblastic Leukemia researchEpigenetics and DNA Methylation

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The novel histone deacetylase inhibitor, LBH589, induces expression of DNA damage response genes and apoptosis in Ph− acute lymphoblastic leukemia cells

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Scuto, Anna, Kirschbaum, Mark, Kowolik, Claudia, Kretzner, Leo, Juhasz, Agnes, Atadja, Peter, Pullarkat, Vinod, Bhatia, Ravi, Forman, Stephen, Yen, Yun, Jove, Richard·2008·Blood

DOI 10.1182/blood-2007-10-117762PMC PMC2384136

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Abstract

We investigated the mechanism of action of LBH589, a novel broad-spectrum HDAC inhibitor belonging to the hydroxamate class, in Philadelphia chromosome-negative (Ph(-)) acute lymphoblastic leukemia (ALL). Two model human Ph(-) ALL cell lines (T-cell MOLT-4 and pre-B-cell Reh) were treated with LBH589 and evaluated for biologic and gene expression responses. Low nanomolar concentrations (IC(50): 5-20 nM) of LBH589 induced cell-cycle arrest, apoptosis, and histone (H3K9 and H4K8) hyperacetylation. LBH589 treatment increased mRNA levels of proapoptosis, growth arrest, and DNA damage repair genes including FANCG, FOXO3A, GADD45A, GADD45B, and GADD45G. The most dramatically expressed gene (up to 45-fold induction) observed after treatment with LBH589 is GADD45G. LBH589 treatment was associated with increased histone acetylation at the GADD45G promoter and phosphorylation of histone H2A.X. Furthermore, treatment with LBH589 was active against cultured primary Ph(-) ALL cells, including those from a relapsed patient, inducing loss of cell viability (up to 70%) and induction of GADD45G mRNA expression (up to 35-fold). Thus, LBH589 possesses potent growth inhibitory activity against including Ph(-) ALL cells associated with up-regulation of genes critical for DNA damage response and growth arrest. These findings provide a rationale for exploring the clinical activity of LBH589 in the treatment of patients with Ph(-) ALL.

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Research works printed but not linked: 1

Scuto, 2004, Synergistic cytotoxic effects of a combination of a novel tyrosine kinase inhibitor AMN107 and histone deacetylase inhibitor LBH589 against Bcr-Abl expressing human leukemia cells [abstract]., Blood (ASH Annual Meeting Abstracts), 104, 546a

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Authors: Scuto, A., Kirschbaum, M., Kowolik, C., Kretzner, L., Juhasz, A., Atadja, P., Pullarkat, V., Bhatia, R., Forman, S., Yen, Y., & Jove, R.
Affiliations: City Of Hope National Medical Center (US)
Novartis Pharmaceuticals, Cambridge, MA
ORCID: Juhasz, Agnes
Pullarkat, Vinod
Bhatia, Ravi
Forman, Stephen
Yen, Yun
Venue: Blood
Publisher: American Society of Hematology
Published: 2008-05-15
Volume: 111
Issue: 10
Pages: 5093-5100
ISSN: 0006-4971 (ISSN-L)
1528-0020
DOI: 10.1182/blood-2007-10-117762
PMC: PMC2384136
OpenAlex: W2086799752
Cited by: 141
References: 53
Citations by year: 2026: 1 · 2025: 3 · 2024: 2 · 2023: 7 · 2022: 9 · 2021: 10 · 2020: 13 · 2019: 9 · 2018: 5 · 2017: 4 · 2016: 7 · 2015: 6 · 2014: 8 · 2013: 8 · 2012: 15
FWCI: 4.39
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Blood (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: W. M. Keck Foundation
National Institutes of Health
National Cancer Institute (R01CA055652)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Histone Deacetylase Inhibitors Research
Health Sciences › Medicine › Hematology › Acute Lymphoblastic Leukemia research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
Keywords: panobinostat, histone deacetylase inhibitors, Philadelphia chromosome-negative acute lymphoblastic leukemia, DNA damage response, apoptosis, GADD45G, histone acetylation, H2AX phosphorylation, FOXO3, cell cycle arrest, MOLT-4 cells, REH cells, relapsed leukemia
MeSH terms: Panobinostat, GADD45 Proteins, Acetylation, DNA Damage, Gene Expression Regulation, Histones, Humans, Hydroxamic Acids, Indoles, Tumor Cells, Cultured, Apoptosis, Intracellular Signaling Peptides and Proteins, Precursor Cell Lymphoblastic Leukemia-Lymphoma

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The novel histone deacetylase inhibitor, LBH589, induces expression of DNA damage response genes and apoptosis in Ph− acute lymphoblastic leukemia cells

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